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1,294 results for “hemodynamics”
The Role of Somatostatin in the Hemodynamics of the Hepatic Circulation in Patients Undergoing Liver Resection
ClinicalTrials.gov study NCT04010669. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Normal Reference Values in Han Adults of Extremity Arterial Structure and Hemodynamics by High-frequency Ultrasound
ClinicalTrials.gov study NCT05970926. IPD Sharing: NO. Countries: 0. Publications: 0.
Microarray-based gene expression of rabbit basilar artery smooth muscle cells exposed to hemodynamic insult
GEO Series GSE61212. Oryctolagus cuniculus. 6 samples. Type: Expression profiling by array.
Dataset related to article "Hemodynamics in AVF over time: A protective role of vascular remodeling toward flow stabilization"
<p>Dataset containing magnetic resonance images, blood flow boundary conditions and post-processing of computational fluid simulations results</p>
Dataset related to the article "The potential of sound analysis to reveal hemodynamic conditions of arteriovenous fistulae for hemodialysis"
<p>The dataset contains a folder for each patient including for each follow-up:</p> <p>- MR images used to generate the 3D AVF model for the computational fluid dynamic simulations</p> <p>- US images used to derive the AVF patient-specific boundary conditions for the computational fluid dynamic simulations</p> <p>- AVF sound recordings</p> <p>- Two files containing the post-processing of simulation results (cross-sectional areas of the AVF vessels and the surface map of the Oscillatory Shear Index)</p>
Dataset related to article "Arteriovenous fistula creation with VasQ device: A feasibility study to reveal hemodynamic implications"
<p>The dataset contains two folders: 1) Imaging, and 2) Post-processing, each containing data from individual patients (C1, C2, V1, and V2).</p> <p>In details:</p> <p>- the Imaging folder contains MRI DICOM data at different time points (3 days, 3 weeks, and 1 year) and US data used as boundary conditions for CFD simulations</p> <p>- the Post-processing folder contains .vtp files of both morphology (CSA.vtp) and hemodynamics (hemo.vtp) at different time points</p>
ActiveCare+SFT Hemodynamic Profile Compare to SCD Express in Ventilated Patients
ClinicalTrials.gov study NCT00338819. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Effects of Inhibition of NO-Synthesis on Renal Hemodynamics and Sodium Excretion in Patients With Essential Hypertension and Healthy Controls
ClinicalTrials.gov study NCT00345150. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Effects of Acute L-NMMA Treatment on Renal Hemodynamics and Vasoactive Hormones in Patients With Congestive Heart Failure
ClinicalTrials.gov study NCT00344734. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Raw data: Role of cardiopulmonary exercise test in the prediction of hemodynamic impairment in patients with pulmonary arterial hypertension
<p>Periodic repetition of right heart catheterization (RHC) in pulmonary arterial hypertension (PAH) can be challenging. We evaluated the correlation between RHC and cardiopulmonary exercise test (CPET) aiming at CPET use as a potential noninvasive tool for hemodynamic burden evaluation. One hundred and forty‐four retrospective PAH patients who had performed CPET and RHC within 2 months were enrolled. The following analyses were performed: (a) CPET parameters in hemodynamic variables tertiles; (b) position of hemodynamic parameters in the peak end‐tidal carbon dioxide pressure (P<sub>ET</sub>CO<sub>2</sub>) versus ventilation/carbon dioxide output (VE/VCO<sub>2</sub>) slope scatterplot, which is a specific hallmark of exercise respiratory abnormalities in PAH; (c) association between CPET and a hemodynamic burden score developed including mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), cardiac index, and right atrial pressure. VE/VCO<sub>2</sub> slope and peak P<sub>ET</sub>CO<sub>2</sub> significantly varied in mPAP and PVR tertiles, while peak oxygen uptake (peak VO<sub>2</sub>) and O<sub>2</sub> pulse varied in the tertiles of all hemodynamic parameters. P<sub>ET</sub>CO<sub>2</sub> versus VE/VCO<sub>2</sub> slope showed a strong hyperbolic relationship (<em>R</em> <sup>2</sup> =&thinsp;0.7627). Patients with peak P<sub>ET</sub>CO<sub>2</sub> > median (26 mmHg) and VE/VCO<sub>2</sub> slope < median (44) presented lower mPAP and PVR (p < 0.005) than patients with peak P<sub>ET</sub>CO<sub>2</sub> < median and VE/VCO<sub>2</sub> slope > median. Multivariate analysis individuated peak VO<sub>2</sub> (<em>p</em> =&thinsp;0.0158) and peak P<sub>ET</sub>CO<sub>2</sub> (<em>p</em> =&thinsp;0.0089) as hemodynamic score independent predictors; the formula 11.584 − 0.0925 × peak VO<sub>2</sub> − 0.0811 × peak P<sub>ET</sub>CO<sub>2</sub> best predicts the hemodynamic score value from CPET data. A significant correlation was found between estimated and calculated scores (<em>p</em> < 0.0001), with a precise match for patients with mild‐to‐moderate hemodynamic burden (76% of cases). The results of the present study suggest that CPET could allow to estimate the hemodynamic burden in PAH patients.</p> <p> </p>
PREVALENCE AND CLINICAL OUTCOME OF MAIN ECHOCARDIOGRAPHIC AND HEMODYNAMIC HEART FAILURE PHENOTYPES IN A POPULATION OF HOSPITALIZED PATIENTS 70 YEARS OLD AND OLDER
<p><strong>BACKGROUND</strong>: Heart failure (HF) echocardiographic and hemodynamic categories are poorly characterized in the elderly. We aimed to evaluate the prevalence and clinical outcomes of echocardiographic and hemodynamic HF phenotypes in a consecutive series of hospitalized patients aged ≥70 years.</p> <p><strong>METHODS: </strong>All consecutive patients ≥70 years old discharged from the Internal Medicine Unit of our Hospital with a diagnosis of HF, between January and November 2020, entered this retrospective study. All patients underwent physical examination, complete blood tests, chest-X ray and transthoracic echocardiography. At 1-year follow-up, we evaluated the occurrence of the composite outcome of all‐cause mortality and re-hospitalization.</p> <p><strong>RESULTS</strong>: 261 patients (86.3±6.4 yrs, 60.9% women) were retrospectively analyzed. From the study group, 106 “old” (70-84 yrs) and 155 “oldest-old” (≥85 yrs) patients were separately analyzed. A total of 169 (64.7%) patients reported the composite outcome during follow-up: 41 (15.7%) died and 128 (49.0%) were re-hospitalized. At 1-year follow-up, survival analysis did not show any statistically significant difference between age groups (p = 0.31) and between HF echocardiographic categories (p=0.34), whereas HF patients with “cold-dry” phenotype had significantly poorer survival compared to the other hemodynamic subtypes (p<0.001). Male sex (HR 1.44, 95%CI 1.04-1.98), “cold-dry” phenotype (HR 3.90, 95%CI 1.73-8.77), high sodium level (HR 1.03, 95%CI 1.01-1.04) and low estimated glomerular filtration rate (eGFR) (HR 0.98, 95%CI 0.97-0.99) were independently associated with the outcome occurrence.</p> <p><strong>CONCLUSIONS: </strong>Male sex, “cold-dry” phenotype, high sodium level and low eGFR are the main adverse prognostic indicators over a mid-term follow-up in hospitalized patients aged ≥70 yrs.</p>
Impact of Sacubitril/Valsartan on surfactant binding protein, central sleep apnea, lung function tests and heart failure biomarkers: hemodynamic or pleiotropism?
<p><strong>Purpose:</strong> Little is known about the mechanism underlying Sacubitril/Valsartan effects in patients with heart failure (HFrEF). Aim of the study is to assess hemodynamic vs. non-hemodynamic Sacubitril/Valsartan effects by analyzing several biological and functional parameters.</p> <p><strong>Methods: </strong>Seventy-nine patients (86% males, age 66±10 years) were enrolled. At baseline and 6 months after reaching the maximum Sacubitril/Valsartan tolerated dose, we assessed biomarkers, transthoracic echocardiography, polysomnography, spirometry, and carbon monoxide diffusing capacity of the lung (DLCO).</p> <p><strong>Results:</strong> Mean follow-up was 261±41 days with 83% of patients reaching Sacubitril/Valsartan maximum dose (97/103mg b.i.d). Significant improvements were observed in cardiac performance and biomarkers: left ventricular ejection fraction increased (31±5 vs. 37±9 %; p<0.001), end-diastolic and end-systolic volumes decreased; NT-proBNP decreased (1196 [IQR 648-2891] vs. 958 [IQR 424-1663] pg/ml; p<0.001) in parallel with interleukin ST-2 (28.4 [IQR 19.4-36.6] vs. 20.4 [IQR 15.1-29.2] ng/ml; p<0.001) and circulating surfactant binding proteins (proSP-B: 58.43 [IQR 40.42-84.23] vs. 50.36 [IQR 37.16-69.54] AU; p=0.014 and SP-D: 102.17 [IQR 62.85-175.34] vs. 77.64 [IQR 53.55-144.70] AU; p<0.001).</p> <p>Forced expiratory volume in 1 second and forced vital capacity improved. DLCO increased in the patients’ subgroup (n=39) with impaired baseline values (from 65.3±10.8 to 70.3±15.9 %predicted; p=0.013). We also observed a significant reduction in central sleep apneas (CSA).</p> <p><strong>Conclusion</strong>: Sacubitril/Valsartan effects share a double pathway: hemodynamic and systemic. The first is evidenced by NT-proBNP, proSP-B, lung mechanics, and CSA improvement. The latter is confirmed by an amelioration of DLCO, ST-2, SP-D as well as by reverse remodeling echocardiographic parameters.</p>
Post-operative and mid-term hemodynamic changes after replacement of the ascending aorta
<p>To evaluate aortic distensibility and pulse waveform patterns associated with the ascending aortic aneurysm, and to analyze the postoperative and mid-term hemodynamic changes induced by prosthetic replacement of the ascending aorta. Central blood pressure waves were recorded at the carotid artery level by means of a validated transcutaneous arterial tonometer in 30 patients undergoing prosthetic replacement of ascending aortic aneurysm and in 30 control patients. Measurements were obtained the day before surgery and 5 to 7 days and 16 to 20 months after surgery. The ascending aortic aneurysm was associated with a less steep slope of early systolic phase of the pressure curve (pulsus tardus) compared with a control group (0.54 ! 0.18 mm Hg/ms vs 0.69 ! 0.26 mm Hg/ms; P .011). Replacing the ascending aorta with a noncompliant vascular prosthesis steepened the pulse pressure slope during the early systolic phase in the postoperative period (0.77 ! .29 mm Hg/ms), providing values comparable with those of the control group in the mid-term (0.67 ! .20 mm Hg/ms). No change in aortic stiffness was found either postoperatively or in the mid-term after ascending aorta surgical replacement (carotid-femoral pulse wave velocity: preoperative, 9.0 ! 2.6 m/s; postoperative, 9.0 ! 2.9 m/s; mid-term postoperative, 9.3 ! 2.8 m/s). This study does not con!rm the assumption that substitution of the viscoelastic ascending aorta with a rigid prosthesis can cause serious hemodynamic alterations downstream, because we did not observe a worsening of global aortic distensibility after insertion of a rigid prosthetic aorta. The ascending aortic aneurysm is associated with a pulsus tardus.</p>
Current Limitations of Invasive Exercise Hemodynamics for the Diagnosis of Heart Failure With Preserved Ejection Fraction
<p>raw data ex-hemo protocol</p>
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